In the present study, rather than assessing MPS, our interest was

In the present study, rather than assessing MPS, our interest was primarily Alvocidib nmr focused on the extent with which 10 g of whey protein comprised of 5.25 EAAs would affect the activity of the Akt/mTOR pathway after resistance exercise when compared to carbohydrate alone and if this activity might also be systemically affected

by either insulin or IGF-1. The reason for our interest was an attempt to discern if the 5.25 g of EAAs contained within 10 g of whey protein, without carbohydrate, was adequate to activate the Akt/mTOR compared to carbohydrate in response to a single bout of resistance exercise. Our interest was heightened by a previous study in which albumin protein intake at 10 g (4.3 g EAAs) significantly increased MPS, and maximally MK-2206 molecular weight when 20 g (8.6 g EAAs) and 40 g (16.4 g EAAs) were ingested, yet none of the three concentrations had any affect on the activities of the

Akt/mTOR pathway intermediates S6K1 (Thr389), rps6 (Ser240/244), or eIF2Bε (Ser539) at 60 and 240 min post-exercise [10]. Despite previous evidence indicating otherwise [10], we were curious to determine if 10 g of whey protein would produce increases in other key Akt/mTOR signalling intermediates following resistance exercise. It is evident that acute resistance exercise results in a significant increase in the rate of initiation of protein synthesis compared with resting muscle [33]. It is suggested that signal transduction pathways control the rate of initiation of MPS, and appear to be the key factors in the hypertrophic process [34, 35]. Of particular importance is the complex myriad of signaling proteins, with Akt suggested to be a key selleck compound regulator. Maximal activation of Akt occurs through phosphorylation of Ser473 and it appears that Akt may have a relatively short period of activation after an acute bout of resistance exercise [36]. Research into the regulation Sunitinib of Akt signalling by exercise has produced conflicting

results. A series of studies have demonstrated that contractile activity either positively or negatively regulates Akt activity [15, 37–39], while others failed to find any change [40–42]. In the current study, we found that resistance exercise and nutrient ingestion failed to induce a significant change in the phosphorylation of Akt. Stimuli of the Akt pathway includes hormones and muscle contraction. Insulin [43] and IGF-I [44] bind to their respective membrane-bound receptors and subsequently activate phosphatidylinositol-3 kinase (PI-3K), an upstream activator for Akt phosphorylation. Quantification of circulating IGF-I levels has yielded inconsistent results, with levels being reported to decline [45], increase [46], or remain unchanged [47] after the onset of exercise. Furthermore, circulating IGF-1 has been shown to have no direct effect on muscle hypertrophy [48].

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